Sukehiko Kawashima

Body surface distributions of ST segment changes after exercise in effort angina pectoris without myocardial infarction.

To investigate the sites of exercise-induced ST segment changes on the body surface in effort angina pectoris without myocardial infarction, we performed 87-lead ECG mapping in 61 patients before and 1.5 and 5 minutes after treadmill exercise. ST segment depression most often occurred in the left anterior chest leads and ST segment elevation developed mainly in the right upper chest leads. There was a good correlation between the number of lead points that showed ST segment depression (nSTd) and the number of those that showed ST segment elevation (nSTe) 1.5 minutes after exercise (r = 0.92). From 1.5 to 5 minutes after exercise, changes in nSTd for individual patients correlated well with changes in nSTe (r = 0.89). It was suggested that the ST segment elevation observed in this study directly reflected the subendocardial ischemia of the left ventricle. In patients with one-vessel disease (n = 32), there was wide overlap in the sites of ST segment changes among patients with left anterior descending artery disease (n = 19), those with left circumflex artery disease (n = 6), and those with right coronary artery disease (n = 7). These findings should lead to a better understanding of exercise-induced ST segment changes for the diagnosis of coronary artery disease.

Non-invasive detection of coronary artery disease by body surface electrocardiographic mapping after dipyridamole infusion†

Electrocardiographic changes after dipyridamole infusion (0.568 mg/kg/4 min) were studied in 41 patients with coronary artery disease and compared with those after submaximal treadmill exercise by use of the body surface mapping technique. Patients were divided into three groups; 19 patients without myocardial infarction (non-MI group), 14 with anterior infarction (ANT-MI) and eight with inferior infarction (INF-MI). Eighty-seven unipolar electrocardiograms (ECGs) distributed over the entire thoracic surface were simultaneously recorded. After dipyridamole, ischemic ST-segment depression (0.05 mV or more) was observed in 84% of the non-MI group, 29% of the ANT-MI group, 63% of the INF-MI group and 61% of the total population. Exercise-induced ST depression was observed in 84% of the non-MI group, 43% of the ANT-MI group, 38% of the INF-MI group and 61% of the total. For individual patients, there were no obvious differences between the body surface distribution of ST depression in both tests. The increase in pressure rate product after dipyridamole was significantly less than that during the treadmill exercise. The data suggest that the dipyridamole-induced myocardial ischemia is caused by the inhomogenous distribution of myocardial blood flow. We conclude that the dipyridamole ECG test is as useful as the exercise ECG test for the assessment of coronary artery disease.

Inhibition of dipyridamole-induced myocardial ischemia by diltiazem in patients with coronary artery disease

Summary: We investigated the effect of diltiazem on dipyridamole-induced myocardial ischemia in eight patients with coronary artery disease. Dipyridamole was infused at a rate of 0.142 mg/kg/min for 4 min, and 87-lead mapping was performed to determine the number of leads with ischemic ST-segment depression ≥0.05 mV (nST). The range of nST was 8–24 (mean, 13.8) in the control study. Of eight patients studied, a single dose of 90 mg diltiazem administered 3 h before dipyridamole infusion inhibited dipyridamole-induced ST-segment depression completely in seven (nST = 0) and incompletely in one (nST = from 24 to 5). It was concluded that diltiazem could suppress the myocardial ischemia following dipyridamole infusion.